Abstract

Cardiac ischemia can present as distinctive clinical syndromes such as acute myocardial infarction, cardiogenic shock, sudden cardiac arrest or chronic congestive heart failure. All of the clinical syndromes share common pathophysiological events including reduction of cardiac output and systemic oxygen delivery (DO2) and activation of neurohumoral stress response. The balance between systemic DO2 and oxygen consumption (VO2) is maintained by modification of systemic oxygen utilization and demands which are essential for tissue viability and survival in cardiac ischemic syndromes. Low blood flow and the neurohumoral response may influence cellular metabolism (e.g., acute ischemia preconditioning and chronic downregulation of aerobic metabolism) and microcirculatory perfusion patterns to decrease systemic oxygen demands and VO2 in harmony with low cardiac output and systemic DO2. The clinical relevance of these metabolic adaptations and their influence on the outcome in cardiac ischemic syndromes remains unknown.

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